1,721,276 research outputs found

    AT1 receptor blockade and renal protection

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    It is well known that, if there has been sufficient initial damage due to any cause, chronic renal insufficiency usually progresses, even when the original disease is no longer active. Hypertension and proteinuria are the main factors affecting chronic renal insufficiency progression. In the past years, it has been shown that ACE-inhibitors have antihypertensive and antiproteinuric capacity and can also be renoprotective partially independently to these effects. AT1 receptor antagonists (AT1RA) inhibit the renin-angiotensin system by selectively blocking the AT1 subtypes of angiotensin II receptors, without affecting, unlike ACE-inhibitors, bradykinin metabolism. Several experimental studies have confirmed that the acute renal effects of AT1RA on hemodynamics are partially different from ACE-inhibitors, because they do not dramatically reduce the resistance of the efferent arteriole. In non-hemodynamically-based animal models of renal injury, it is still unclear why AT1RA, unlike ACE-inhibitors, are partially ineffective in preserving renal morphology; in other animal models the long- term renoprotective effects of AT1RA are comparable to ACE-inhibitors. The antihypertensive and antiproteinuric effects of AT1RA have been confirmed in humans. However, the clinical impact of this new class of drugs in slowing the rate of chronic renal insufficiency progression needs to be assessed by means of prospective long-term randomized trials which are still ongoing. The hypothesis that AT1RA in association with ACE-inhibitors may allow additive renoprotection is extremely fascinating

    Flow Cytometry Immunophenotyping for the Evaluation of Bone Marrow Dysplasia

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    The pathological hallmark of myelodysplastic syndromes (MDS) is marrow dysplasia, which represents the basis of the WHO classification of these disorders. This classification provides clinicians with a useful tool for defining the different subtypes of MDS and determining individual prognosis. The WHO proposal has raised some concern regarding minimal diagnostic criteria particularly in patients with normal karyotype without robust morphological markers of dysplasia (such as ring sideroblasts or excess of blasts). Therefore, there is clearly a need to refine the accuracy to detect marrow dysplasia. Flow cytometry (FCM) immunophenotyping has been proposed as a tool to improve the evaluation of marrow dysplasia. Rationale for the application of FCM in the diagnostic work up of MDS is that immunophenotyping is an accurate method for quantitative and qualitative evaluation of hematopoietic cells and that MDS have been found to have abnormal expression of several cellular antigens. To become clinically applicable, FCM analysis should be based on parameters with sufficient specificity and sensitivity, data should be reproducible between different operators and the results should be easily understood by clinicians. In this report, we reviewed the most relevant progresses in detection of marrow dysplasia by FCM in MDS as defined by WHO criteria

    Dialysate calcium concentration during calcimimetic treatment: a neglected issue

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    Hypocalcaemia is a well-known effect of the treatment of secondary hyperparathyroidism when using calcimimetics. In a retrospective, observational, study, which was published recently in this Journal [1], Louie et al. investigated the frequency, predictors, and consequences of cinacalcetinduced hypocalcaemia in a cohort of over one thousand haemodialysis patients. They found that hypocalcaemia occurred in more than two third of the treated patients and was mild in many cases. Nonetheless, in one third it was moderate (1.87– < 2.0 mmol/L; 23%) or even severe (< 1.87 mmol/L; 9%). These results coming from a “realworld” setting raise questions on the true potentially negative impact of hypocalcaemia per se or of its treatment, including the increase of dialysate calcium concentration

    Flow cytometry immunophenotyping for the evaluation of bone marrow dysplasia.

    No full text
    The pathological hallmark of myelodysplastic syndromes (MDS) is marrow dysplasia, which represents the basis of the WHO classification of these disorders. This classification provides clinicians with a useful tool for defining the different subtypes of MDS and determining individual prognosis. The WHO proposal has raised some concern regarding minimal diagnostic criteria particularly in patients with normal karyotype without robust morphological markers of dysplasia (such as ring sideroblasts or excess of blasts). Therefore, there is clearly a need to refine the accuracy to detect marrow dysplasia. Flow cytometry (FCM) immunophenotyping has been proposed as a tool to improve the evaluation of marrow dysplasia. Rationale for the application of FCM in the diagnostic work up of MDS is that immunophenotyping is an accurate method for quantitative and qualitative evaluation of hematopoietic cells and that MDS have been found to have abnormal expression of several cellular antigens. To become clinically applicable, FCM analysis should be based on parameters with sufficient specificity and sensitivity, data should be reproducible between different operators and the results should be easily understood by clinicians. In this report, we reviewed the most relevant progresses in detection of marrow dysplasia by FCM in MDS as defined by WHO criteria
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